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Mechanisms of stimulus‐evoked intracellular acidification in frog nerve fibres
Author(s) -
Khodorov B.,
Valkina O.,
Turovetsky V.
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)80253-x
Subject(s) - chemistry , ouabain , blockade , biophysics , stimulation , intracellular , tetrodotoxin , veratridine , stimulus (psychology) , sciatic nerve , intracellular ph , grenouille , sodium , endocrinology , anatomy , biochemistry , sodium channel , salientia , biology , receptor , psychology , organic chemistry , psychotherapist , xenopus , gene
Measurements of cytoplasmic pH (pH i ) in frog nerve fibers (sciatic nerve and its thin bundles) were performed by using fluorescein diacetate. Earlier it had been established that veratridine (VER) treatment of the nerve greatly enhances the stimulus‐evoked intracellular acidification (SEIA) which becomes irreversible after blockade of the Na + /K + pump with ouabain. Present experiments have shown that inhibition of lactic acid production by iodacetamide (5 mM) or blockade of Cl − influx by SITS do not prevent or attenuate the VER‐ and stimulus‐evoked decrease in pH i . Blockade of Na + /H + exchange by EIPA impedes pH i recovery following repetitive stimulation. Lowering of external pH (pH e ) to 6.5 enhances, while elevation of pH e to 9.5 greatly diminishes SEIA, both in the presence or absence of VER. The hypothesis is put forward that SEIA results from excessive influx of H + and Na + into the fiber via activated Na + channels: internal Na + suppresses Na + /H + exchange which potentiates the pH i decrease caused by H + influx.